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CARDIO

  1. Which embryological structure becomes the following adult structure?

    Ascending aortal and pulmonary trunk
    Truncus arteriosus
  2. Which embryological structure becomes the following adult structure?

    Coronary sinus
    L horn of sinus venosus
  3. Which embryological structure becomes the following adult structure?

    Superior Vena Cava
    R cardinal veins
  4. Which embryological structure becomes the following adult structure?

    Smooth parts of L and R ventricles
    Bulbis cordis
  5. Which embryological structure becomes the following adult structure?

    Smooth part of R atrium
    R horn of sinus venosus
  6. Which embryological structure becomes the following adult structure?

    Trabeculated L and R atrium
    primitive atria
  7. Which embryological structure becomes the following adult structure?

    Trabeculated parts of L and R ventricles
    primitive ventricles
  8. What structure divides the truncus arteriosus into the aortic and pulmonary trunks? What is its cellular origin?
    Spiral septum - aka the aorticopulmonary septum from neural crest cells
  9. What fetal vessel has the highest oxygenation?
    Umbilical vein
  10. What causes the ductus arteriosus to close?
    Indomethacin, increased O2 and decreased prostaglandins
  11. What causes the foramen ovale to close?
    increased Left Atrium pressure due to infant breathing
  12. What is the most common congenital cardiac anomaly?
    VSD
  13. What are the components of tetralogy of fallot?
    PROV

    • Pulmonary stenosis
    • RVH
    • Overriding aorta
    • VSD

    boot shaped heart, cyanotic spells
  14. explain how the great vessels are attached in a transposition of the great vessels.
    • Aorta to Right ventricle
    • Pulmonary Trunk to Left Ventricle
  15. A 45 year old male presents with a BP of 160/90 on the right arm and 170/92 on the left arm. Ther eare no palpable pulses in the feet. What problem does this patient most likely have?
    Coarctation of the aorta
  16. Describe blood flow through the PDA
    • Left to right shunt
    • aorta to pulmonic circulation
  17. What heart defect is associated with the following disorder?

    Chromosome 22q11 deletions
    Truncus arteriosus, tetralogy of fallot
  18. What heart defect is associated with the following disorder?

    Down syndrome
    ASD, VSD, AV septal defects

    "endocardial cushion defects"
  19. What heart defect is associated with the following disorder?

    Congenital Rubella
    PDA, Pulmonary Stenosis, Septal defects
  20. What heart defect is associated with the following disorder?

    Turner's Syndrome
    Coarctation of the Aorta
  21. What heart defect is associated with the following disorder?

    Marfan's syndrome
    Aortic insufficiency
  22. What problems are offspring of diabetic mothers at higher risk for?
    Transposition of the great vessels, erb duchenne, shoulder dystocia, hypoglycemia
  23. What is the pulse pressure in a patient with a systolic BP of 150 and a MAP of 90?
    MAP = 2/3 diastolic + 1/3 systolic

    90=X + 50

    X = 40

    • Diastolic = 60
    • Systolic = 150
    • Pulse pressure is Sys = Dia
    • 150-60 = 90mmHg
  24. what is the basic equation for cardiac output? What is the Fick principle?
    CO = SV x HR

    Fick: CO = O2 consumption / [arterial O2 - venous O2)
  25. what increases a hearts contractility?
    • Catecholamines
    • Increased intracellular Ca2+
    • Decreased extracellular Na+
    • Digitalis
  26. what decreases a hearts contractility?
    • B blockers
    • heart failure
    • acidosis
    • hypoxia/hypercapnia (decreased PO2, increased PCO2)
    • CCB's (nondhydropyridine)
  27. How can the myocardial O2 demand be decreased during an ischemic heart event?
    • B blockers
    • ACE inhibitors
    • Nitro

    anything that decreases afterload, contractility and HR.
  28. what is the formula for mean arterial pressure?
    MAP = CO x TPR

    MAP = 2/3 dia + 1/3 sys
  29. what is the formula for SV?
    SV = EDV - ESV
  30. What factors affect stroke volume?
    • afterload
    • preload
    • contractility
  31. what is the ejection fraction?
    EF = SV/EDV
  32. preload is approximately what? It's affected by what type of drug?
    the ventricular end diastolic volume

    VENOdilators - Nitroglycerin

    less blood back to the heart = less preload
  33. afterload is approximately equal to what? it's affected by what type of drug?
    the mean arterial pressure

    VASOdilators - Hydralazine

    dilates arteries, decreases pressure against which the heart must pump
  34. What pushes the Starling Curve to the Left? to the Right?
    • Image Upload 2
    • Exercise Left (greater stroke volume)
    • CHF right (fluid overload, low SV)
  35. What are the signs of right sided heart failure?
    • Edema
    • JVD
    • Nutmeg liver
    • Peripheral signs
  36. what are the signs of left sided heart failure?
    • dyspnea on exertion
    • cardiac dilation
    • orthopnea
    • paroxysmal nocturnal dyspnea
  37. how does poor cardiac output result in an increase in aldosterone?
    JG cells in the kidney sense a decrease in BP -> secrete renin -> angiotensin -> angiotensin II -> vasoconstriction -> aldosterone secretion
  38. What medications reduce mortality in a CHF patient?
    • ACE inhibitors
    • Spironolactone
    • Loop Diuretics
    • Thiazide
    • Metoprolol or Carvedilol
  39. what medications are used to treat acute heart failure?
    • Furosemide
    • Morphine
    • Nitrates
    • O2
  40. What is the mechanism of action of the cardiac glycosides?
    Blocks Na+/K+ATPase which increases intracellular Ca2+ and decreases extracellular Na+
  41. What is seen on points 1-5?

    Image Upload 4
    • 1 - normal operating point of the heart
    • 2 - exercise (low TPR)
    • 3 - hemorrhage (high TPR)
    • 4 - CHF
    • 5 - Mean Systemic Pressure
  42. Describe the cardiac cycle

    Image Upload 6
    • a) mitral valve opens - rapid filling
    • b) mitral valve closes - isovolumetric contraction - pressure building
    • c) aortic valve opens - systolic ejection - pressure still increases
    • d) aortic valve closes - isovolumetric relaxation - pressure drop
  43. Describe the S1, S2, S3 and S4 heart sounds
    • 1 is eMpTy
    • 2 is hAPpy

    • S1 - mitral and tricuspid closure
    • S2 - aortic and pulmonary closure

    • Pathologic:
    • S3 - early diastole - CHF (increased filling pressure)
    • S4 - late diastole - "atrial kick" LVH
  44. Describe the JVP waves
    • a - RA contraction
    • c - RV contraction
    • v - RA filling
  45. What causes pitting edema vs non pitting edema?
    Pitting - water only swelling

    Non-pitting - water and protein in the interstitium
  46. what causes wide splitting of the S2 sound?
    • pulmonic stenosis
    • Right BBB
  47. what causes fixed splitting of the S2 sound?
    ASD (pulmonic closure delay)
  48. what causes paradoxical splitting of the S2 sound?
    • aortic stenosis
    • Left BBB
  49. What do you hear on ausculation: A
    Systolic ONLY

    • Aortic stenosis
    • (flow murmur)
  50. What do you hear on ausculation: P
    Systolic Ejection ONLY

    • Pulmonic stenosis
    • (flow murmur)
  51. What do you hear on ausculation: T
    Pansystolic

    • Tricuspid Regurg
    • VSD

    • Diastolic
    • Tricuspid Stenosis
    • ASD
  52. What do you hear on ausculation: M
    Systolic

    Mitral Regurg

    Diastolic

    Mitral Stenosis
  53. What do you hear on ausculation: Left Sternal Border
    Systolic

    Hypertrophic Cardiomyopathy

    Diastolic

    • Aortic Regurgitation
    • Pulmonic Regurgitation
  54. What heart sounds do you hear during systole?
    Aortic and Pulmonic Stenosis

    Mitral and Tricuspid Regurg
  55. What heart sounds do you hear during diastole?
    Aortic and Pulmonic Regurg

    Mitral and Tricuspid Stenosis
  56. Identify the Murmur:

    holosytolic, high pitched blowing murmur, loudest at apex and radiates toward axilla
    Mitral Regurg
  57. Identify the murmur:

    holosytolic, high pitched blowing murmur, loudest at tricuspid area, radiating to right sternal border
    Tricuspid regurg
  58. Identify the murmur:

    crescendo-decrescendo systolic ejection murmur with ejection click.
    Aortic Stenosis
  59. what are the main causes of aortic stenosis?
    • 1 - bicuspid aortic valve
    • 2 - calcifications
  60. Identify the murmur:

    holosystolic harsh sounding murmur loudest at tricuspid area.
    VSD

    hard to distinguish from tricusp regurg
  61. Identify the murmur:

    late systolic crescendo with midsystolic click
    Mitral valve prolapse

    most common
  62. Identify the murmur:

    high pitched blowing diastolic murmur, wide pulse pressure, bounding pulses, head bobbing
    Aortic regurg
  63. Identify the murmur:

    follows opening snap, late diastolic murmur
    Mitral stenosis
  64. Identify the murmur:

    continuous machine like murmur
    PDA
  65. Describe the phases of the ventricular action potential:

    Image Upload 8
    • Phase 0 - Na+ open
    • Phase 1 - Na+ inactive, K+ open
    • Phase 2 - plateau - Ca2+ open, release from SR
    • Phase 3 - Ca2+ close, K+ influx
    • Phase 4 - K+ leak open
  66. Describe the pacemaker action potential:

    Image Upload 10
    • Phase 4 - K+ open, Na+ open
    • Phase 0 - Na+ inactivated, Ca2+ open
    • Phase 3 - Ca2+ inactivated, K+ open
  67. In which phase of the pacemaker action potential are B blockers effective? CCB's? When does the AV node transmission get prolonged?
    • B blockers - phase 4
    • CCB's - phase 0

    AV node prolonging transmission = Phase 0
  68. EKG:

    what does the P wave represent?
    atrial depolarization
  69. EKG representation and timing:

    PR interval
    conduction delay through the AV node

    0.2 seconds
  70. EKG representation and timing:

    QRS complex
    ventricular depolarization

    0.12 seconds
  71. EKG representation and timing:

    QT interval
    ventricle contraction

    0.4 seconds
  72. EKG representation and timing:

    T wave
    ventricular repolarization
  73. when is an inverted T wave seen?
    recent MI
  74. when is a U wave seen?
    hypokalemia, bradycardia
  75. Put in order of speed of conduction:
    AV node
    atria
    ventricles
    Purkinje fibers
    Purkinje fibers > atria > ventricles > AV node
  76. Name the pacemakers
    • SA node
    • AV node
    • bundle of His
    • Purkinje
    • Ventricles
  77. Describe the conduction pathway
    • SA node
    • atria
    • AV node
    • common bundle
    • LAF
    • bundle branches
    • Purkinje fibers
    • ventricles
  78. Image Upload 12
    Identify. What causes it?
    Torsades de Pointes

    • anything that prolongs the QT interval
    • can progress to V fib
  79. Image Upload 14
    Identify. How do you treat?
    A fib - irregularly irregular with no P waves

    Tx: Cardioversion w/in 24 hours. Otherwise, B blockers, CCB's, digoxin, prophylactic warfarin

    can cause pulmonary embolism
  80. Image Upload 16
    Identify. How do you treat?
    Atrial Flutter (sawtooth)

    Tx: Class Ia, Ic or III antiarrhytmics
  81. Image Upload 18
    Identify. Prolonged PR interval. What can cause this?
    1st degree AV block

    HTN, Lyme Disease
  82. Image Upload 20
    Identify: progressive PR lengthening warning
    2nd degree AV block Type I

    warning before drops
  83. Image Upload 22
    Identify: No warning lengthening of pR interval
    2nd degree AV block Type II

    no warning before drops
  84. Identify: P waves bear no relation to QRS complexes Tx with pacemaker, assoc with Lyme Disease
    3rd degree AV block
  85. Identify: completely erratic rhythm with no identifiable waves
    V fib
  86. this is released from the atria in response to increased blood volume and atrial pressure.

    escape from aldosterone mechanism
    atrial natiuretic peptide
  87. the aortic arch transmits via this nerve to the medulla in response to elevated blood pressure ONLY
    Vagus nerve
  88. the carotid sinus transmits via this nerve to this nucleus in the medulla responding to any change in BP.
    glossopharyngeal nerve

    solitary nucleus
  89. what do baroreceptors do?
    sense hypotension and cause vasoconstriction

    can be massaged to decrease the heart rate
  90. Peripheral chemoreceptors respond to what, compared to central chemoreceptors?
    Peripheral - decreased PO2, increased PCO2, and decreased pH of blood (acidosis)

    Central - changes in pH and PCO2 in brain interstitial fluid
  91. The pulmonary capillary wedge pressure is a good approximation of what?
    left atrial pressure
  92. pulmonary vasculature is unique in that hypoxia causes _ so that only well ventilated areas are perfused. This is opposite of all other organs.
    Vasoconstrict

    typically hypoxia causes vasodilation
  93. Pc = capillary pressure...what does this do?
    pushes fluid out of capillary
  94. Pi = interstitial fluid...what does this do?
    pushes fluid out of interstitium (into capillary)
  95. Image Upload 24c = plasma colloid osmotic pressure...what does this do?
    pulls fluid into capillary

    "salty plasma"
  96. Image Upload 26i = interstitial fluid colloid osmotic pressure...what does this do?
    pulls fluid into interstitium

    "salty interstitium"
  97. What is the equation for net filtration pressure?
    Pnet = [(Pc-Pi) - (Image Upload 28c-Image Upload 30i)]
  98. Kf is what?
    filtration constant (capillary permeability)
  99. CHF causes edema by a change in what capillary starling force?
  100. increased capillary pressure - pushing water out of the vessel
  101. Nephrotic syndrome or liver failure causes edema by a change in what capillary starling force?
    decreased plasma proteins (leaking out of kidneys)

    this means watery blood that diffuses out into the tissues following their gradient
  102. Toxins, infections and burns cause edema by what starling force?
    increased Kf - filtration constant
  103. Lymphatic blockage causes edema by a change in what capillary starling force?
    increased interstitial fluid colloid osmotic pressure. salty interstitium pulls water out into the tissues
  104. this disease is associated with delta waves in the EKG and can result in SVT. Treatment for it includes Procainamide specifically.
    Wolff-Parkinson-White
  105. What are the Right to Left Shunts? The 5 T's
    • Tetralogy of Fallot
    • Transposition of the great vessels
    • Truncus Arteriosus
    • Tricuspid Atresia
    • Total anomalous pulmonary venous return (pulmonary veins drain into right sided circulation)
  106. what is a persistent truncus arteriosus?
    failure to divide into pulmonary trunk and aorta
  107. what are the left to right shunts?
    • VSD - most common
    • ASD
    • PDA
  108. uncorrected septal defect causes compensatory pulmonary vascular hypertrophy -> pulmonary hypertension. As pulmonary resistance increases the shunt reverses from Left to Right to Right to Left which causes late cyanosis (clubbing and polycythemia)
    Eisenmenger's Syndrome
  109. Coarctation of the aorta - infantile type. Describe.
    aortic stenosis proximal to insertion of ductus arteriosus.
  110. Coarctation of the aorta - adult type. describe
    stenosis distal to the ligamentum arteriosum.

    • notching of ribs
    • hypertension in upper extremities
    • hypotension in lower extremities

    can result in aortic regurg

    most commonly associated with bicuspid aortic valve
  111. what keeps a PDA open? what closes it? what can uncorrected PDA lead to?
    open - prostaglandins

    closed - indomethacin

    late cyanosis in lower extremities
  112. What are some signs of hyperlipidemia?
    • Atheromas (plaques in blood vessel walls)
    • Xanthomas (plaques of fat in skin
    • Tendon xanthoma - achilles
    • Corneal arcus - fat in cornea
  113. What type of arteriosclerosis?

    calcification in the media. usually benign does not obstruct blood flow
    Monckeberg
  114. What type of arteriosclerosis?

    hyaline thickening of small arteries in essential hypertension or diabetes mellitus. hyperplastic "onion skinning" in malignant hypertension
    Arteriolosclerosis
  115. What type of arteriosclerosis?

    fibrous plaques and atheromas in intima of arteries major arteries - elastic, large and medium muscular
    Atherosclerosis
  116. how does atherosclerosis progress?
    endothelial damage, macrophage and LDL accumulation, foam cell formation, fatty streaks, PDGF and TGF-B recruit smooth muscle cells, fibrous plaques, complex atheromas
  117. describe the pathology of an abdominal vs thoracic aortic aneurysm
    • abd - atherosclerosis, male smokers > 50
    • thoracic - HTN, marfan's
  118. longitudinal intraluminal tear forming a false lumen. associated with tearing chest pain and radiation to the back. CXR shows mediastinal widening.
    Aortic dissection
  119. What is the difference between a type a and a type b aortic dissection?
    type a - radiates to front, involves arch and ascending aorta - require surgery

    type b - radiates to back, involves descending aorta - B blockers to treat
  120. Contrast the 3 types of angina
    stable - atherosclerosis, ST depression on EKG tx: nitro

    Printzmetals - coronary artery spasm, ST elevation on EKG tx: nifedipine

    unstable - thrombosis but no necrosis, ST depression on EKG
  121. what is the most common cause of sudden cardiac death?
    v fib
  122. MI evolution - gross appearance, microscopic, risk associated
    0-4 hours
    no gross or microscopic appearance change, risk of arrhythmia
  123. MI evolution - gross appearance, microscopic, risk associated

    4-12 hours
    dark mottling

    early coagulative necrosis, edema, hemorrhage

    arrhythmia risk
  124. MI evolution - gross appearance, microscopic, risk associated

    12-24 hours
    dark mottled tissue

    contraction bands, neutrophils arrive

    risk of arrhythmia
  125. MI evolution - gross appearance, microscopic, risk associated

    2-4 days
    red tissue

    neutrophil emigration, massive necrosis

    risk of arrhythmia
  126. MI evolution - gross appearance, microscopic, risk associated

    5-10 days
    yellow

    granulation tissue

    Free wall rupture, tamponade, papillary muscle rupture, interventricular septum rupture (macrophage degradation)
  127. MI evolution - gross appearance, microscopic, risk associated

    7 weeks
    white tissue

    contracted scar

    Ventricular aneurysm (popping out)
  128. Diagnosis of MI: name expected markers and when they rise, also diagnostic gold standard
    EKG is the gold standard

    Troponin I rises after 4 hours - stays for 7-10 days - most specific

    CKMB - useful for diagnosing "reinfarction"
  129. What does ST elevation, ST depression and pathologic Q waves tell you?
    Q waves and ST Elevation - transmural infarct

    ST depression - angina or subendocardial infarct
  130. ECG diagnosis - Leads with Q waves:

    V1-V4
    LAD - anterior wall infarct
  131. ECG diagnosis - Leads with Q waves:

    V1-V2 only
    LAD - Anteroseptal infarct
  132. ECG diagnosis - Leads with Q waves:

    V4-V6
    LCX - Anterolateral
  133. ECG diagnosis - Leads with Q waves:

    I, aVL
    LCX - Lateral wall infarct
  134. ECG diagnosis - Leads with Q waves:

    II, III and aVF
    RCA - Inferior wall infarct
  135. this is an autoimmune disorder resulting in fibrinous pericarditis post MI
    Dressler's Syndrome
  136. Most common cardiomyopathy. Findings include S3, dilated heart on ultrasound, balloon appearance on CXR. Systolic Eccentric Hypertrophy
    Dilated (Congestive) Cardiomyopathy
  137. What are the etiologies of Dilated Cardiomyopathy?
    • Alcohol abuse
    • Beriberi
    • Coxsackie B virus
    • Cocaine use
    • Chagas Disease
    • Doxorubicin toxicity
    • Hemochromatosis
  138. Hypertrophy of IV septum too close to mitral valve leading to outflow obstruction. Autosomal dominant, associated with Friedrich's Ataxia, S4, normal sized heart, apical impulses, systolic murmur.
    Hypertrophic cardiomyopathy

    Most common cause of sudden death in young athletes. Tx: BB or Verapamil
  139. major causes include sarcoidosis, amyloidosis, postradiation or endocardial fibroelastosis, Loffler's syndrome (eosinophilic infiltrate), hemochromatosis.
    Restrictive obliterative cardiomyopathy
  140. CHF caused by Left Heart Failure:
    • Pulmonary edema
    • Paryoxysmal nocturnal dyspnea
    • Orthopnea
  141. CHF caused by Right Heart Failure:
    • Hepatomegaly
    • Ankle and Sacral Edema
    • Jugular Venous Distension
  142. enlargement of the right ventricle due to high blood pressure in the lungs
    Cor Pulmonale
  143. _ sided heart failure results in pulmonary symptoms
    Left - backs up into lungs from left heart
  144. _ sided heart failure results in edema, JVD and liver back up
    Right sided
  145. Fever, Roth spots, Oslers nodes, new murmur, Janeway lesions, anemia, Splinter hemorrhages.
    Bacterial endocarditis
  146. what valves are most often impacted in bacterial endocarditis
    mitral valve

    IV drug users - tricuspid valve
  147. What bug causes acute bacterial endocarditis? subacute?
    acute - S. aureus

    subacute - S. viridans
  148. Endocarditis can also be due to what 2 bugs besides S. aureus and S. viridans?
    Enterococci (S. bovis)

    S. epidermidis (IV drug users)
  149. Verrucous sterile vegetations on the valves, associated with SLE, usually benign
    Libman - Sachs endocarditis

    SLE causes LSE!
  150. What are the culture negative organisms that can cause Bacterial Endocarditis?
    HACEK Organisms

    • Haemophius
    • Actinobacillus
    • Cardiobacterium
    • Eikenella
    • Kingella
  151. Fever, erythema marginatum, valvular damage, elevated ESR, red hot joints (migratory polyarthritis), subcutaneous nodules, chorea. Immune mediated type II hypersensitivity disease.
    Rheumatic fever
  152. a consequence of pharyngeal infection with Group A strep. MVP seen, then mitral stenosis later in life. Aschoff bodies and Anitschkow's cells and elevated ASO titers seen
    Rheumatic fever
  153. What is an Aschoff body?
    granuloma with giant cells
  154. What is an Anitschkow cell?
    activated histiocytes
  155. What are the three different types of acute pericarditis?
    Fibrinous - most common - loud friction rub

    Serous - noninfectious inflammatory (SLE, Rheumatic fever)

    Suppurative/Purulent - infectious
  156. compression of heart by fluid in the pericardium. shows with hypotension, increased JVD, distant heart sounds, increased heart rate, pulsus paradoxus
    Cardiac tamponade
  157. a decrease in amplitude of systolic blood pressure by 10mmHg during inspiration.

    Seen in: cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup
    Pulsus paradoxus
  158. tree bark appearance of the aorta due to infectious disruption of the vasa vasorum
    syphilitic heart disease
  159. A left atrial _ is the most common primary cardiac tumor in adults. Described as a "ball-valve" obstruction.
    Myxoma
  160. The most common heart tumor overall is _
    mets from melanoma or lymphoma
  161. the most frequent primary cardiac tumor seen in kids is _ and it's associated with tuberous sclerosis (which is associated with what two other diseases?)
    Cardiac rhabdoymoma

    • astrocytoma
    • angiomyolipoma
  162. AV malformation in small vessels is called what?
    telangiectasias
  163. what are some causes of cardiogenic shock?
    • MI
    • CHF
    • PE
    • Arryhtmias
    • Cardiac tamponade
    • Tension PTX
  164. what other severe problems often coexist in septic shock patients?
    • DIC
    • acute renal failure
    • acute pancreatitis
    • ARDS
    • liver failure
    • adrenal insufficiency
    • interstitial ileus
  165. Vasculitis: Unilateral headache, jaw claudication, elderly females. May cause irreverisble blindness, associated with polymyalgia rheumatica (joint pain). Tx high dose steroids
    Temporal arteritis
  166. Vasculitis: Pulseless disease, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbance, elevated ESR - seen in asian women.
    Takayasu's arteritis
  167. Vasculitis: seen in young adults. associated with Hep B, fever, weight loss, malaise, headache. Typically involves renal arteries, Immune complex. Tx: steroids, cyclophosphamide
    Polyarteritis nodosa
  168. Vasculitis: asian children < 4 years old, fever, lymphadenitis, strawberry tongue, hand-foot erythema and desquamation. Tx: IV Ig and Aspirin
    Kawasaki disease
  169. Vasculitis: heavy smokers, male <40 y/o, claudication, gangrene, Raynauds.

    How do you treat?
    Buerger's disease

    Stop smoking!
  170. Vasculitis: pauci-immune glomerulonephritis, p-ANCA and mpo-ANCA positive
    Microscopic polyangitis
  171. Vasculitis: URI, LRI, Renal - hematuria and red cell casts. Multinucleated giant cells. Triad of 1) focal necrotizing vasculitis, 2) necrotizing granulomas in lung and upper airway, 3) necrotizing glomerulonephritis. c-ANCA positive
    Wegener's Granulomatosis
  172. Vasculitis: seen with asthma, sinusitis, palpable purpura, wrist/foot drop (periph neurop). Granulomatous vasculitis with eosinophilia - p-ANCA positive.
    Churg Strauss syndrome
  173. Vasculitis: childhood systemic vasculitis, IgA complexes, IgA nephropathy following URI - palpable purpura on legs/butt, arthralgia, abdominal pain, melena.
    Henoch-Schonlein Purpura (palpable purpura following URI)
  174. congenital vascular disorder that affects capillarys. Port wine stain, AVM in brain, seizures, early onset glaucoma, mental retardation
    Sturge Weber Disease

    "Port Wine Stain"
  175. Vascular tumors: benign capillary hemangioma regresses spontaneously.
    Strawberry hemangioma
  176. Vascular tumors: benign in elderly, does not regress
    Cherry hemangioma
  177. Vascular tumors: capillary hemangioma that can ulcerate and bleed - assoc with trauma and pregnancy
    Pyogenic granuloma
  178. Vascular tumors: cavernous lymphangioma of the neck associated with Turner Syndrome
    Cystic Hygroma
  179. Vascular tumors: Painful red blue tumor under fingernails
    Glomus tumor
  180. benign capillary papules in AIDS patients caused by Bartonella henselae infections. NOT Kaposi's.
    Bacillary angiomatosis
  181. Vascular tumors: Highly lethal malignancy of liver. Associated with exposures - vinyl chloride, arsenic and ThO2
    Angiosarcoma of the Liver
  182. Vascular tumor:

    Lymphatic malignancy associated with persistant lymphedema
    Lymphangiosarcoma
  183. Vascular tumors: Endothelial malignancy associated with HIV and HH8
    Kaposi's sarcoma
  184. Hydralazine: MOA, Use, Tox
    MOA: increas cGMP - arteriole vasodilation

    Use: HTN - first line in pregnancy with a methyldopa

    Tox: reflex tach, Lupus like syndrome
  185. CCB's: Names, MOA, Use, Tox
    Nifedipine, verapamil, diltiazem, amlodipine

    • MOA: block calcium channels (L-type)
    • Verapamil best for heart calcium channels, Nifedipine best for smooth muscle calcium channels.

    Use: HTN, Angina, Raynauds

    Tox: AV block, edema, flushing, constipation
  186. How do you treat malignant hypertension?
    Nitroprusside - increases cGMP -> NO

    Fenoldopam - D1 agonist

    Diazoxide - K+ channel opener (hyperpolarization)
  187. Nitroglycerin: MOA, Use, Tox
    MOA: vasodilate by releasing NO causing increase in cGMP

    Use: Angina

    Tox: reflex tach, flushing, "Monday disease"
  188. What drugs cause drug induced lupus?
    SHIP!

    • Sulfasalazine
    • Hydralazine
    • Isoniazid
    • Procainamide
  189. Combo of what two drugs is most effective in treating angina?
    Nitrates and B blockers
  190. Statins: MOA, Main effect, Tox, Notes
    MOA: HMG-CoA reductase inhibitor - inhibits cholesterol synthesis

    Main: Decrease LDL

    Tox: Hepatotox, Rhabdomyolysis
  191. Niacin: MOA, Main effect, Tox, Notes
    MOA: inhibits lipolysis in adipose, reduces VLDL secretion into tissues

    Main Effect: Increase HDL

    Tox: Flushing (decreased by aspirin), Hyperglycemia, Hyperuricemia
  192. Bile Acid Resins: Names, MOA, Main Effect, Tox, Notes
    Names: Cholestyramine, Colestipol, Colesevelam

    MOA: prevent reabsorption of bile acids

    Main: lower LDL

    Tox: GI discomfort, gallstones
  193. Ezetimibe: MOA, Main Effect, Tox
    MOA: Prevents cholesterol reabsorption at small intestine brush border

    Main: lower LDL

    Tox: rare increase in LFT's
  194. Fibrates: Name, MOA, Main Effect, Tox
    Gemfibrozil, clofibrate, bezafibrate, fenofibrate

    MOA: upregulate LPL to increase TG clearance

    Main Effect: decrease Trigylcerides

    Tox: myositis, hepatotox, cholersterol gallstones
  195. Digoxin: MOA, Use, Tox, Antidote
    MOA: Na+/K+ ATP ase inhibitor

    Use: CHF, A fib

    • Tox: cholinergic, increased PR, decreased QT, T wave inversion, arrhythmia, hyperkalemia
    • worsened by renal failure

    Antidote: lidocaine, anti-dig FAB fragments
  196. Nesiritide: MOA, Use, Tox
    MOA: recombinant B type natriuretic peptide, increase in vasodilation

    Use: diagnose CHF, acute CHF

    Tox: Hypotension
  197. Antiarrhythmics: Class Ia: Name, MOA, Tox
    "Double Quarter Pounder"...

    Disopyramide, Quinidine, Procainamide

    MOA: Na+ channel blocker

    Tox: quinidine - headache and tinnitus. procainamide - lupus like reaction.

    General: thrombocytopenia, torsades de pointes
  198. Antiarrhythmics: Class Ib: Name MOA Tox
    "Lettuce, Tomato, Pickles, Mayo..."

    Lidocaine, Tocainide, Phenytoin, Mexiletine

    MOA: Na+ channel blocker

    Tox: CNS and CV depression

    IB is BEST for MI
  199. Antiarrhytmics: Class Ic: Name, MOA, Tox
    "Fries, Please".

    Flecainide, Propafenone

    MOA: Na+ channel blocker

    Tox: arrhythmias

    IC is contraindicated in MI
  200. Antiarrhythmics: Class II - MOA, Clin Use, Tox
    MOA: Beta blockers! Propranolol, Esmolol, Atenolol, Timolol

    Use: V tach, SVT (esmolol), A fib, A flutter

    Tox: impotence, exacerbation of asthma

    Treat OD with glucagon
  201. Antiarrhytmics: Class III - MOA, Use, Tox
    K IS BAD

    Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide

    MOA: K+ channel blockers

    Use: antiarrhythmic

    Tox: Amiodarone - pulmonary fibrosis, hyper/hypothyroidism, hepatotoxicity, photosensitivity
  202. Which drug has all class effects?
    Amiodarone
  203. Antiarrhytmics: Class IV - MOA, Use, Tox
    Verapamil, diltiazem

    MOA: Ca2+ channel blockers

    Tox: constipation, flushing, edema, AV block
  204. Adenosine: MOA, Use, Tox
    MOA: increase K+ efflux

    Use; SVT

    Tox: flushing, hypotension
  205. Mg is effective in treating what two things?
    Torsades de points and digoxin toxicity
Author
cherubicsiren
ID
157427
Card Set
CARDIO
Description
CARDIO
Updated

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